The proposed research has a goal of defining the relationship between chronic progressive renal disease and exposure to environmental hydrocarbon solvents. Clinical studies have established a relationship between human glomerulonephritis and hydrocarbon solvent exposure, in addition to the well known acute renal tubular toxicity of many of these agents. This study will attempt to produce an animal model of hydrocarbon-induced glomerulonephritis in rats by chronic intraperitoneal administration of common petroleum distillates and hydrocarbon solvents. Gasoline, carbon tetrachloride, toluene, trichloroethylene and a degreasing solvent, stanisol, will be studied regarding their glomerulotoxic and nephrotoxic potential. The mechanism of induced injury will be studied by examining tissue with light, immunofluorescence and electron microscopy. N,N'-diacetylbenzidine has been shown to produce a proliferative glomerulonephritis in rats. We propose to study the pathogenesis of this glomerulonephritis which is morphologically similar to a form of human glomerulonephritis mediated by immune mechanisms. The role of the immune system in potentiating this toxin-induced glomerulonephritis will be studied by light, immunofluorescence and electron microscopy of renal tissue, as well as by a search for serum anti-kidney antibodies. If immunologic mechanisms are involved in perpetuating glomerulonephritis, this would explain why many cases of human glomerulonephritis are apparently mediated by immune mechanisms, but the antigens stimulating the immune response are unknown.